Cambridge Neuroscience Public Lecture in association with the BNA with Professor Russell Foster: 'Light, Clocks and Sleep'

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Description: Cambridge Neuroscience in association with the British Neuroscience Association was delighted to welcome Professor Russell Foster from the University of Oxford to deliver the public neuroscience lecture at the annual Cambridge Neuroscience Seminar, which was held on March 20th at the Babbage Lecture Theatre in Cambridge. Russell Foster is Professor of Circadian Neuroscience and Head of the Nuffield Laboratory of Ophthalmology at the University of Oxford. Russell's research interests span the neurosciences but are currently focused upon two broad themes. The first relates to how environmental light is detected and processed by vertebrate photoreceptors. The second line of research relates to how circadian rhythms and sleep are generated and their disruption in mental illness and neurodegenerative disease.
 
Created: 2012-03-23 12:41
Collection: Cambridge Neuroscience
'Light, Clocks and Sleep'
Cambridge Neuroscience
Publisher: University of Cambridge
Copyright: Dr D. Glynn
Language: eng (English)
Keywords: circadian; photoreceptor; eye; neuroscience; clocks;
 
Abstract: Light, Clocks and Sleep: The Discovery of a New Photoreceptor within the Eye
Until the late 1990’s it seemed inconceivable to most vision biologists that there could be an unrecognised class of light sensor within the eye. After all, the eye was the best understood part of the central nervous system. One hundred and fifty years of research had explained how we see: Light is detected by the rods and cones of the retina and their responses are assembled into an “image” by inner retinal neurones, followed by advanced visual processing in the brain. This representation of the eye left no room for an additional class of ocular photoreceptor. However, work in a variety of animals, including mice and humans, overturned this conventional view of the eye. We now know that the rods and cones are not alone.

Most organisms possess a 24h biological (circadian) clock, which acts to ‘fine-tune’ physiology and behaviour to the varying ecological demands of the day/night cycle. Such a clock is only useful if biological time remains synchronised to solar time, and the daily change in the gross amount of light (irradiance) at dawn or dusk provides the most reliable indicator of the time of day. In mammals the “master clock” is located within small paired nuclei at the base of the brain called the suprachiasmatic nuclei (SCN). The SCN receive direct retinal projections which adjust the clock to the light/dark cycle, and eye loss in mammals blocks this completely. We were interested in how the eye detects light to provide this re-setting signal. Surprisingly, we found that visually blind mice, with genetic defects in the rods and cones, could still use their eyes to regulate the clock. These, and a host of subsequent experiments including studies in humans with genetic defects of the eye, showed that the processing of light information by the circadian and classical visual systems is different and that the mammalian eye contains an additional non-rod, non-cone photoreceptor based upon a small number of photosensitive retinal ganglion cells (pRGCs). The pRGCs have unusual light-sensing properties and use a remarkable light sensitive molecule called “melanopsin” for this task. We also know that these pRGCs do a lot more than regulate the clock, and are involved in a host of other irradiance detecting tasks that regulate sleep, alertness, hormonal rhythms and even pupil constriction. As a result these findings the clinical diagnosis of blindness is being revised. We now appreciate that eye loss will plunge an individual into a world that lacks both vision and a sense of time.
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